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1 antly faster diffusion of CD14 compared with TLR2.
2 a RING E3-ubiquitin ligase, associates with TLR2.
3 om knockout mice for NE (ela(-/-)), TLR4, or TLR2.
4 entiation and function through engagement of TLR2.
5 y and repair gene signature via the receptor TLR2.
6 r, through the TLR4/MD2 receptor complex and TLR2.
7 corresponding to HLA-DQA1, HLA-DQA2, OLR1 or TLR2.
8 was demonstrated to be partially mediated by TLR2.
10 bers and 5-HT levels, whereas treatment with TLR2/1 agonist upregulates 5-HT production in irradiated
12 locks TLR2 dimerization that is critical for TLR2/1 and TLR2/6 heterodimer signaling to blunt inflamm
15 We found that the TLR2/6 heterodimer, not TLR2/1, is responsible for CDT recognition, and that gen
17 mmatory cytokine production and release in a TLR2/1-dependent manner, using the TLR1 single-nucleotid
20 volunteers were screened for the presence of TLR2 (2029C/T and 2258G/A), TLR3 (1377C/T, 1234C/T, and
21 cells, IL-12 and CCL2 responses as evoked by TLR2, 3, 4, 5, and 8, as well as IL-12 responses evoked
22 n, initiating local gut inflammation through TLR2/4 activation, resulting in the activation of proinf
26 omotes ubiquitination and degradation of the TLR2/4 adaptor protein TIRAP and TLR2 in macrophages and
28 ollected from 12- to 14-week-old TLR2, TLR4, TLR2/4 double knock-out (KO) mice using a MiSeq platform
31 n the present study, we examined the role of TLR2/4 signaling on various astrocyte functions (i.e., p
33 , Toll-like receptor (TLR)2, TLR4, and both (TLR2/4) to the maintenance of neutrophil homeostasis in
34 Low lnc-IL7R expression in COPD may augment TLR2/4-mediated inflammation and be associated with acut
35 onal antibodies against TNF-alpha suppressed TLR2/4-mediated upregulation of astrocyte proliferation,
37 s including NF-kappaB and MAPK downstream of TLR2/6 are upregulated in mice with intact TLR2/6 signal
38 dimerization that is critical for TLR2/1 and TLR2/6 heterodimer signaling to blunt inflammation in a
42 nses to all Toll-like receptor 1/2 (TLR1/2), TLR2/6, and TLR4 agonists were impaired in the fibroblas
44 lear cells responded normally to all TLR1/2, TLR2/6, TLR4, TLR7, and TLR8 (R848) agonists tested, and
45 s in knockout mice revealed a major role for TLR2, a lesser role for TLR4, a supplementary role for C
52 tory responses through Toll-like receptor 2 (TLR2) activation, and this whether they are bound to nuc
55 We examined whether deficiency of maternal TLR2 affects the normal development of oral tolerance an
57 al cells showed attenuated IL-8 responses to TLR2 agonist despite expressing TLR2 similar to normal,
60 d from the colonic LMMP, incubation with the TLR2 agonist increased the percentage of neurons origina
66 se from human monocytes is stimulated by the TLR2 agonists Pam3CSK4 or FSL-1, as well as the TLR4 ago
70 design and chemistry for the conjugation of TLR2 agonists to antigens, carbohydrates, polymers, and
73 n a mouse model, and the combination of anti-TLR2 and antivascular endothelial growth factor receptor
75 ophages to employ multiple receptors such as TLR2 and CD36 to recognize a single ligand, as in this c
76 or-associated macrophages (TAMs) through the TLR2 and MyD88 pathway, and recruits p62 to activate the
80 in epidermal keratinocytes, soy PG inhibited TLR2 and TLR4 activation and inflammatory mediator expre
82 inflammatory mediator expression induced by TLR2 and TLR4 activators as well as NFkappaB activation
85 he combined, but not the individual, loss of TLR2 and TLR4 increased the replication of beta cells, b
86 t study we show that the toll-like receptors TLR2 and TLR4 inhibited the diet-induced replication of
87 ge in the oral microbial composition in both TLR2 and TLR4 KO mice demonstrate that these TLRs contri
89 e-exposed Toll-like receptors (TLRs) such as TLR2 and TLR4 survey the extracellular environment for p
91 n-mediated regulation of Toll-like receptor (TLR2 and TLR4) signaling in dendritic cells, but not in
92 ctivated Toll-like receptors (TLRs), such as TLR2 and TLR4, dimerize and move laterally across the pl
96 s (Toll-like receptors), we demonstrate that TLR2 and TLR6 are required for the activation of human a
99 ir lipid chains in the hydrophobic cavity of TLR2 and, in some cases, TLR1, at the vicinity of the di
101 ate PD-L1 expression on normal IMC; IMC from Tlr2(-/-) and Tlr7(-/-) mice demonstrated similar result
103 lular matrix was similarly reduced in GF WT, Tlr2(-/-) , and heterozygous Vwf(+/-) mice that are all
105 er host chitin-binding Toll-like receptor 2 (TLR2) and CD14 are required for the anti-inflammatory ef
106 to dissect the role of Toll-like receptor 2 (TLR2) and programmed death-ligand 1 (PD-L1) in regulatin
107 engage human and mouse Toll-like receptor 2 (TLR2) and to inhibit mouse osteoblast differentiation an
108 The level of toll-like receptor 4 (TLR4), TLR2, and erythropoietin-producing hepatoma A2 (EphA2) e
109 matory responses were partially inhibited in TLR2- and TLR4-deficient mice compared to those of wild-
112 and the transmembrane toll-like receptor 2 (TLR2) are important receptors in the plasma membrane of
113 und to be dependent on Toll-like receptor 2 (TLR2), as evident by reduced expression of IRE1alpha and
114 PF triggered activation of NF-kappaB through TLR2, as determined using a variety of TLR-transfected h
115 antibodies against Toll-like receptor (TLR)1/TLR2, as well as small interfering RNA targeting TLR1/TL
119 d C57BL/6 mice, which are reconstituted with Tlr2 (-/-) bone marrow cells, and in germ-free mice.
122 xia in mice with or without functional TRL2 (TLR2(+/+), C57BL/6-Tyrc-Brd-Tg(Tlr2-luc/gfp)Kri/Gaj;TLR2
130 zygous TLR2(+/-) pups from wild-type (WT) or TLR2(-/-) dams were fed either by their biologic dam or
135 OmpU-treated macrophages, p38 activation is TLR2 dependent, but JNK activation happens through a sep
136 to stimulate host cell Toll-like receptor 2 (TLR2)-dependent signaling and interleukin-1beta (IL-1bet
137 eus Cell wall components of S. aureus elicit TLR2-dependent cellular responses, but the exact signali
139 eus infection of human monocytes activates a TLR2-dependent endosomal signaling pathway, leading to I
141 culosis (Mtb LAM) would prime human PMN in a TLR2-dependent manner and investigated this with specifi
145 sponsive cathelicidin expression through the TLR2-dependent p38-MAPK-CYP27B1-VDR signaling pathway.
149 glycine lipid classes were shown to promote TLR2-dependent tumor necrosis factor alpha (TNF-alpha) r
150 ed a TLR2 trans-membrane peptide that blocks TLR2 dimerization that is critical for TLR2/1 and TLR2/6
151 estigated responses to Toll-like receptor 2 (TLR2)-driven extracellular signal-related kinase (ERK) s
152 structure of Diprovocim in a complex with a TLR2 ectodomain, which revealed, unexpectedly, two Dipro
154 ct signaling pathways activated by S. aureus-TLR2 engagement and the consequences of their activation
155 meras and immunohistology, we identified the TLR2-expressing cells involved in this early neutrophil
156 The decreased cytokine responses in R753Q TLR2-expressing macrophages were accompanied by impaired
157 n together, our data show a crucial role for TLR2-expressing nonhematopoietic skin cells in the recru
160 roduction, which mechanistically depended on Tlr2 Finally, we found that TRIM58 mRNA and protein expr
163 stimulation of the Toll-like receptor (TLR)1-TLR2 heterodimer (referred to herein as TLR1/2), TLR7 or
167 immune system through Toll-like receptor 2 (TLR2); however, the pathogen-associated molecular patter
169 ce higher 5-HT production in BON-1 cells via TLR2 in a dose-dependent manner, whereby the effect of e
170 Altogether, these data identify a role for TLR2 in DENV infection and provide insights into the com
171 cascades triggered by stroke and a role for TLR2 in injury, we also used direct TLR2 stimulation as
174 ndings not only suggest an important role of TLR2 in mucosal 5-HT production in the gut by resident m
175 Our results underline a critical role for TLR2 in regulating milk components that are essential fo
176 ary immunopathology of chimeric mice lacking TLR2 in the hematopoietic compartment (TLR2KO-->WT) was
177 ation on the potential benefits of targeting TLR2 in various gut disorders that exhibit aberrant 5-HT
178 egarding its lipid binding and activation of TLR2 indicate that it could participate in the initiatio
180 pigment epithelium cells, ligand binding to TLR2 induced robust expression of proinflammatory cytoki
184 ssarily colocalization, between Dectin-1 and TLR2 is required for their synergistic regulation of mac
188 PHHs are able to sense HBV particles through TLR2, leading to an activation of anti-HBV immune respon
191 pression and release in response to TLR4 and TLR2 ligand stimulation but not for TLR-independent stim
192 lar to that induced by toll-like receptor 2 (TLR2) ligand Pam3Cys, but different from those induced b
193 sis (Mtb), were covalently conjugated to the TLR2-ligand Pam(2)Cys to generate a self-adjuvanting lip
195 In this study, we show that in normal cells, TLR2 limits RV-induced IFN responses by attenuating STAT
196 -27p28 production, when triggered by zymosan/TLR2, LPS/TLR4, or R848/TLR7/8 activation, but selective
197 ctional TRL2 (TLR2(+/+), C57BL/6-Tyrc-Brd-Tg(Tlr2-luc/gfp)Kri/Gaj;TLR2(-/-),C57BL/6-Tlr2tm1Kir).
199 STAT1/STAT2 phosphorylation, indicating that TLR2 may limit RV-induced IFN responses via SIRT-1.
201 the IRE1alpha/XBP1 pathway as a regulator of TLR2-mediated protective innate immune responses in S au
202 t with an HBV entry inhibitor attenuated the TLR2-mediated response to HBV, suggesting a receptor bin
204 findings suggest that resistance to KIM5 in TLR2(-/-) mice is dependent on early immune cell traffic
205 sely, restoring early neutrophil presence in Tlr2(-/-) mice through injection of wild-type neutrophil
210 nstrate that Toll-like receptor 2-deficient (TLR2(-/-)) mice are resistant to septicemic infection by
211 -8 in respiratory epithelial cells through a TLR2-, NF-kB- and MAPK-dependent signalling pathway.
212 mpare the diffusion coefficients of CD14 and TLR2 on the apical and basal membranes of macrophages us
216 culture (ALI) model was used to test whether TLR2 or TLR3 stimulation alters epithelial barrier funct
221 e a significantly improved anti-inflammatory TLR2 peptide and critical insights in its mechanism of a
224 and p65 NF-kappaB, suggesting that the R753Q TLR2 polymorphism alters the functions of the myeloid di
229 y and associated with enhanced expression of TLR2 protein and proinflammatory cyto/chemokine producti
230 s, which showed constitutive upregulation of TLR2 protein, overreacted to a proinflammatory milieu (T
234 tdTomato mice and incubated with agonists of TLR2 (receptor for gram-positive bacteria), TLR4 (recept
236 well as small interfering RNA targeting TLR1/TLR2, reduced the expression of RALDH2 in PN-stimulated
238 e-nucleotide polymorphisms (SNPs) rs5743708 (TLR2), rs4986791 (TLR4), rs361525 (TNFA), rs2430561 (IFN
239 and B. licheniformis PGA both elicited more TLR2 signal than B. anthracis PGA, but only responses to
240 an macrophages responded to S. aureus EVs by TLR2 signaling and activation of NLRP3 inflammasomes thr
242 ion in an arthritic mouse model dependent on TLR2 signaling and in a CSS mouse model dependent on TLR
245 Our findings reveal that the outcome of TLR2 signaling includes an IFN-I response in human monoc
247 obiotic approaches directed towards specific TLR2 signaling processes might be developed for treatmen
249 EV-associated lipoproteins not only mediated TLR2 signaling to initiate the priming step of NLRP3 act
253 usly demonstrated that toll-like receptor 2 (TLR2) signaling is critical for nerve injury-induced act
254 ce arises from Toll-like receptor (TLR) 4 or TLR2 signalling and, in the case of protease allergens,
255 responses to TLR2 agonist despite expressing TLR2 similar to normal, indicating dysregulation in TLR2
256 glycine lipids and that these lipids engage TLR2 similarly to the previously reported serine-glycine
261 , the impact of ERK signaling in response to TLR2 stimulation differs between macrophages and DCs, po
263 onula occludens-1 were upregulated following TLR2 stimulation, and ChIP assay demonstrated altered hi
264 of myeloid cells diverged between tMCAO and TLR2 stimulation, in both models, disruption of CX3CR1-C
266 ation and associated tissue damage following TLR2-stimulation, while ERK-mediated induction of IL-12/
267 reased fibrosis in vivo Furthermore, soluble TLR2 (sTLR2), a negative modulator of TLRs that we detec
268 ed that neuroinflammation and the microglial TLR2-system may act as a core process at the intersectio
269 ally, the modulatory role for the functional TLR2-system was suggested in aetiology of depressive, an
271 potent, synthetic small molecule agonist of TLR2/TLR1 and has shown significant adjuvant activity in
273 und that Diprovocim induced the formation of TLR2/TLR1 heterodimers as well as TLR2 homodimers in vit
274 e investigated how Diprovocim interacts with TLR2/TLR1 through in vitro biophysical, structural, and
275 rity to the canonical lipopeptide ligands of TLR2/TLR1, we investigated how Diprovocim interacts with
278 tokine production triggered by various TLRs (TLR2, TLR3, TLR4, and TLR7), C-type lectin receptors (De
279 development, we determined the frequency of TLR2, TLR3, TLR4, and TLR9 single-nucleotide polymorphis
280 falpha(-/-), Il1alpha(-/-)/Il1beta(-/-), and Tlr2(-/-)/Tlr4(-/-) mice as well as Sprague Dawley rats
284 oral swabs collected from 12- to 14-week-old TLR2, TLR4, TLR2/4 double knock-out (KO) mice using a Mi
287 and suggest that selective targeting of the TLR2/TLR4 pathways may reverse beta cell failure in pati
289 d IL-1R (-/-) or TLR4 (-/-) corneas, but not TLR2 (-/-), TLR5 (-/-), TLR7 (-/-), or TLR9 (-/-), were
292 ed the contribution of Toll-like receptor 2 (TLR2) to host resistance against Mycobacterium tuberculo
294 mmunoproteasome proteolysis, by treatment of TLR2 (Toll-like receptor 2)-engaged and TLR7 (Toll-like
299 immune responses triggered predominantly by TLR2 when their centroid-to-centroid proximity is <500 n
300 Various scaffolds are reported to activate TLR2, which include naturally occurring lipoproteins, sy